Evidence map›Paper›PMID 31402170›Full record

ArticleKidney international2019

Endothelin receptor-A mediates degradation of the glomerular endothelial surface layer via pathologic crosstalk between activated podocytes and glomerular endothelial cells.

Kerstin Ebefors, Robert J Wiener, Liping Yu, Evren U Azeloglu, Zhengzi Yi, Fu Jia, Weijia Zhang, Margaret H Baron, John C He, Börje Haraldsson and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Kidney international, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
5.8field-weighted citation impact, top 3% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 120 citations in OpenAlex.

  1. Pooled it
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  16. Selective endothelin A receptor antagonism in chronic kidney disease: improving clinical application.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025
    Review
  17. Blood Pressure Management Strategies and Podocyte Health.American journal of hypertension · 2025
    Review
  18. Review
  19. Review
  20. Article

12 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 2 countries.

Kerstin EbeforsDepartment of Neuroscience and Physiology, Physiology, University of Gothenburg, Gothenburg, Sweden.
Robert J WienerDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Liping YuDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Evren U AzelogluDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Zhengzi YiDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Fu JiaDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Weijia ZhangDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Margaret H BaronDivision of Hematology and Medical Oncology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York; Department of Cell, Developmental, and Regenerative Biology, Icahn School of Medicine at Mount Sinai, New York, New York; Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, New York, New York.
John C HeDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
Börje HaraldssonDepartment of Neuroscience and Physiology, Physiology, University of Gothenburg, Gothenburg, Sweden.
Ilse DaehnDivision of Nephrology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York. Electronic address: ilse.daenhn@mssm.edu.
Icahn School of Medicine at Mount Sinai · USUniversity of Gothenburg · SE

Funding

Glomerular Cell-Cell Crosstalk and InjuryR01DK097253 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI DAEHN, ILSE SOFIA · 2013 to 2025
$7.3M
Prediction of Major Adverse Kidney Events and Recovery (Pred-MAKER) in COVID-19 PatientsR01DK118222 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI Evren U. AZELOGLU · 2018 to 2026
$4.3M
Glomerular Cell-Cell Crosstalk and InjuryR56DK097253 · NIDDK · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI DAEHN, ILSE SOFIA · 2018 to 2018
$150k
NIDDK NIH HHS R01 DK097253NIDDK NIH HHS R01 DK118222NIDDK NIH HHS R56 DK097253
6 · The paper itself

Abstract

Emerging evidence of crosstalk between glomerular cells in pathological settings provides opportunities for novel therapeutic discovery. Here we investigated underlying mechanisms of early events leading to filtration barrier defects of podocyte and glomerular endothelial cell crosstalk in the mouse models of primary podocytopathy (podocyte specific transforming growth factor-β receptor 1 signaling activation) or Adriamycin nephropathy. We found that glomerular endothelial surface layer degradation and albuminuria preceded podocyte foot process effacement. These abnormalities were prevented by endothelin receptor-A antagonism and mitochondrial reactive oxygen species scavenging. Additional studies confirmed increased heparanase and hyaluronoglucosaminidase gene expression in glomerular endothelial cells in response to podocyte-released factors and to endothelin-1. Atomic force microscopy measurements showed a significant reduction in the endothelial surface layer by endothelin-1 and podocyte-released factors, which could be prevented by endothelin receptor-A but not endothelin receptor-B antagonism. Thus, our studies provide evidence of early crosstalk between activated podocytes and glomerular endothelial cells resulting in loss of endothelial surface layer, glomerular endothelial cell injury and albuminuria. Hence, activation of endothelin-1-endothelin receptor-A and mitochondrial reactive oxygen species contribute to the pathogenesis of primary podocytopathies in experimental focal segmental glomerulosclerosis.

Indexed as

AlbuminuriaAnimalsCapillariesCell CommunicationDisease Models, AnimalDoxorubicinEndothelial CellsEndothelin-1Endothelin A Receptor AntagonistsEndothelin B Receptor AntagonistsEndothelium, VascularHumansKidney GlomerulusMiceMice, TransgenicMicroscopy, Electron, ScanningDoxorubicinEDNRB protein, mouseEndothelin-1Endothelin A Receptor AntagonistsEndothelin B Receptor AntagonistsReactive Oxygen SpeciesReceptor, Endothelin AReceptor, Endothelin BReceptor, Transforming Growth Factor-beta Type ITgfbr1 protein, mousecrosstalkEdn1GECsglomerular ESLglycocalyxpodocytesproteinuriaTGF-βI

Identifiers

PMID31402170
PMCPMC7200072
OpenAlexW2946788069

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.